Autoimmune polyneuropathies arise when nerves are damaged by the body's own immune system. Symptoms of these diseases include numbness, muscle weakness, limb pain, cramping, sensitivity to touch and reduced tendon reflex. In general, autoimmune polyneuropathies can be categorized into demyelinating and axonal neuropathies.
One type of demyelinating neuropathy is chronic inflammatory demyelinating polyneuropathy (CIDP). The prevalence of CIDP is about 9 persons per 100,000 (Laughlin et al, Neurology 73:39 (2009)). However, the prevalence of all types of demyelinating neuropathies is about 20 per 100,000. Another type of demyelinating neuropathy is acute inflammatory demyelinating polyneuropathy (AIDP, Guillain-Barre Syndrome), which has an incidence of 2-3 per 100,000 per year. At least one type of neuropathy is associated with the presence of antibodies directed against myelin-associated glycoprotein (MAG) antibodies.
Autoimmune axonal neuropathies include vasculitic neuropathy, sensory ganglioneuritis (Sjogren's syndrome and other collagen vascular diseases), autoimmune autonomic neuropathy, non-length dependent small fiber neuropathy and paraneoplastic neuropathy.
Corticosteroids and/or immunosuppressants have been used to treat these types of autoimmune neuropathies but new therapies may be more effective when targeted to specific biological molecules that contribute to the development of the neuropathies.